ライフサイエンスコーパス: experimental autoimmune

1 hrough MyD88, and subsequent amelioration of experimental autoimmune arthritis was observed to be an

2 geted metabolomics in plasma of B6 mice with experimental autoimmune encephalitis (EAE) at the chroni

3 In experimental autoimmune encephalitis (EAE), autoimmune T

4 Chronic focal experimental autoimmune encephalitis (EAE)-like lesions

5 e associated with local demyelination during experimental autoimmune encephalitis (EAE).

6 TCH1 activation and attenuates Th17-mediated experimental autoimmune encephalitis (EAE).

7 Administration of 4a in mice suffering from experimental autoimmune encephalitis ameliorates the sev

8 cells were more efficient at protecting from experimental autoimmune encephalitis compared with wild-

9 with monosodium urate and the development of experimental autoimmune encephalitis in mice.

10 -CD4 T-cell aggregates during progression of experimental autoimmune encephalitis substantially enhan

11 17 cell numbers, and they are protected from experimental autoimmune encephalitis, a model for multip

12 nergizes with glucocorticoids in attenuating experimental autoimmune encephalitis, a model of multipl

13 nctions in patients with MS and in mice with experimental autoimmune encephalitis, an animal model fo

14 reased T-cell apoptosis, reduced severity of experimental autoimmune encephalitis, and defective immu

15 At the later stages of MS and experimental autoimmune encephalitis, platelets became e

16 We found that early in MS and experimental autoimmune encephalitis, platelets degranul

17 In the multiple sclerosis model experimental autoimmune encephalitis, TYMP and VEGFA co-

18 with wild-type littermates upon induction of experimental autoimmune encephalitis.

19 Further, RVX-297 prevented murine experimental autoimmune encephalomyelitis (a model of hu

20 ty, but surprisingly confers protection from experimental autoimmune encephalomyelitis (EAE) and does

21 ed in-depth analysis of neurodegeneration in experimental autoimmune encephalomyelitis (EAE) and in i

22 , IFN-beta, NAg, and Alum, for inhibition of experimental autoimmune encephalomyelitis (EAE) and indu

23 a is recognized to play an important role in experimental autoimmune encephalomyelitis (EAE) and perh

24 s a critical cytokine in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and, ost

25 ) of multiple sclerosis (MS) subjects and of experimental autoimmune encephalomyelitis (EAE) animals,

26 We used experimental autoimmune encephalomyelitis (EAE) as a mod

27 y in DCs are resistant to the development of experimental autoimmune encephalomyelitis (EAE) as a res

28 Resolution of established experimental autoimmune encephalomyelitis (EAE) can be a

29 eviously shown that loss of AMPK exacerbates experimental autoimmune encephalomyelitis (EAE) disease

30 In an experimental autoimmune encephalomyelitis (EAE) disease

31 aling in astrocytes reduces inflammation and experimental autoimmune encephalomyelitis (EAE) disease

32 osis triggers the development of spontaneous experimental autoimmune encephalomyelitis (EAE) during a

33 te Smads to inhibit Th17 differentiation and experimental autoimmune encephalomyelitis (EAE) has not

34 ral stem/precursor cells (NPCs) in mice with experimental autoimmune encephalomyelitis (EAE) impairs

35 of murine pathogenic TH17 cells that induce experimental autoimmune encephalomyelitis (EAE) in anima

36 Using experimental autoimmune encephalomyelitis (EAE) in C57BL

37 exaggerated T cell responses and spontaneous experimental autoimmune encephalomyelitis (EAE) in mice

38 rime antigen-specific T cells and exacerbate experimental autoimmune encephalomyelitis (EAE) in mice.

39 y T (Treg) cells, abrogates the induction of experimental autoimmune encephalomyelitis (EAE) in rhesu

40 a primate model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE) in the c

41 Following experimental autoimmune encephalomyelitis (EAE) inductio

42 Experimental autoimmune encephalomyelitis (EAE) is a val

43 sly, we showed that the sexual dimorphism in experimental autoimmune encephalomyelitis (EAE) is assoc

44 TLR signaling in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) is uncle

45 ll as PLP138-151-induced relapsing-remitting experimental autoimmune encephalomyelitis (EAE) mice.

46 y in a rat model of arthritis and in a mouse experimental autoimmune encephalomyelitis (EAE) model of

47 els in which BBB was disrupted, including an experimental autoimmune encephalomyelitis (EAE) model of

48 Using the experimental autoimmune encephalomyelitis (EAE) model, w

49 pact of Notch signaling in macrophages in an experimental autoimmune encephalomyelitis (EAE) model.

50 in driving chronic pain in MS using a mouse experimental autoimmune encephalomyelitis (EAE) model.

51 We used the experimental autoimmune encephalomyelitis (EAE) models i

52 HA synthesis, on disease progression in the experimental autoimmune encephalomyelitis (EAE) mouse mo

53 on multiple sclerosis development, using the experimental autoimmune encephalomyelitis (EAE) mouse mo

54 xN-induced model and, in the T cell-mediated experimental autoimmune encephalomyelitis (EAE) mouse mo

55 Experimental autoimmune encephalomyelitis (EAE) represen

56 of the protein kinase CK2 (CK2) ameliorates experimental autoimmune encephalomyelitis (EAE) severity

57 T cell responses in the CxLNs and modulated experimental autoimmune encephalomyelitis (EAE) severity

58 n oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) using Ah

59 Accordingly, TH17 cell-associated experimental autoimmune encephalomyelitis (EAE) was grea

60 To model CNS infiltration by B cells, experimental autoimmune encephalomyelitis (EAE) was indu

61 d a comorbid model system in which mice with experimental autoimmune encephalomyelitis (EAE) were adm

62 We tested this using a model of experimental autoimmune encephalomyelitis (EAE) with hip

63 lination of the CNS have been explored using experimental autoimmune encephalomyelitis (EAE), a CD4 T

64 agy-related gene 7 (Atg7) in DCs ameliorated experimental autoimmune encephalomyelitis (EAE), a CD4 T

65 ction in vivo and attenuated the severity of experimental autoimmune encephalomyelitis (EAE), a disea

66 Experimental autoimmune encephalomyelitis (EAE), a model

67 letion does not benefit clinical symptoms in experimental autoimmune encephalomyelitis (EAE), a model

68 ats, vitamin D supplementation protects from experimental autoimmune encephalomyelitis (EAE), a model

69 the transcription factor Bhlhe40 to mediate experimental autoimmune encephalomyelitis (EAE), a mouse

70 We examined CD48 expression and function in experimental autoimmune encephalomyelitis (EAE), a mouse

71 ucts (FHES) attenuated the clinical signs of experimental autoimmune encephalomyelitis (EAE), a mouse

72 rine (NE) in macrophages and thereby limited experimental autoimmune encephalomyelitis (EAE), a mouse

73 and TH17 cells mediate neuroinflammation in experimental autoimmune encephalomyelitis (EAE), a mouse

74 By studying the role of IRF8 in experimental autoimmune encephalomyelitis (EAE), a mouse

75 nd that Toso(-/-) mice do not develop severe experimental autoimmune encephalomyelitis (EAE), a mouse

76 UV light suppresses experimental autoimmune encephalomyelitis (EAE), a widel

77 ological correlates in Dark Agouti rats with experimental autoimmune encephalomyelitis (EAE), a widel

78 no effect on the development or severity of experimental autoimmune encephalomyelitis (EAE), althoug

79 R knockout mice had more disease severity in experimental autoimmune encephalomyelitis (EAE), an anim

80 iR-146a-deficient mice developed more severe experimental autoimmune encephalomyelitis (EAE), an anim

81 the effects and mechanism of action of Ba in experimental autoimmune encephalomyelitis (EAE), an anim

82 evelopment, in adulthood, and in response to experimental autoimmune encephalomyelitis (EAE), an anim

83 helper cells (Th) during the development of experimental autoimmune encephalomyelitis (EAE), an anim

84 derivative, was shown to reduce severity of experimental autoimmune encephalomyelitis (EAE), an anim

85 of multiple sclerosis (MS), its animal model experimental autoimmune encephalomyelitis (EAE), and neu

86 ts a role for IL-1 in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), but how

87 d in a severe, nonresolving atypical form of experimental autoimmune encephalomyelitis (EAE), charact

88 on partially and inhibits the development of experimental autoimmune encephalomyelitis (EAE), deletio

89 ase multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), expansi

90 s with multiple sclerosis (MS) and mice with experimental autoimmune encephalomyelitis (EAE), inflamm

91 ion of RORgammat prevents TH17 cell-mediated experimental autoimmune encephalomyelitis (EAE), it also

92 multiple sclerosis (MS) and the animal model experimental autoimmune encephalomyelitis (EAE), little

93 ease of the CNS, and in its mouse model, the experimental autoimmune encephalomyelitis (EAE), miRNA d

94 short as six amino acids are therapeutic in experimental autoimmune encephalomyelitis (EAE), reducin

95 tiation 4-positive (CD4(+)) T cells promotes experimental autoimmune encephalomyelitis (EAE), the ani

96 Experimental autoimmune encephalomyelitis (EAE), the ani

97 esent two major pathogenic T cell subsets in experimental autoimmune encephalomyelitis (EAE), the ani

98 c GR deletion in pregnant animals undergoing experimental autoimmune encephalomyelitis (EAE), the ani

99 In both multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), the C-C

100 ultiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), the mec

101 ht to determine the specific role of TSPO in experimental autoimmune encephalomyelitis (EAE), the mos

102 n anti-CD19 mAb, therapeutically ameliorates experimental autoimmune encephalomyelitis (EAE), the mou

103 on of T helper (Th) 17 cells and exacerbated experimental autoimmune encephalomyelitis (EAE), the pri

104 We used a murine model of MS, experimental autoimmune encephalomyelitis (EAE), to eval

105 During experimental autoimmune encephalomyelitis (EAE), wild-ty

106 ide [T20K]kalata B1 using the MS mouse model experimental autoimmune encephalomyelitis (EAE).

107 bates the clinical phenotype of the MS model experimental autoimmune encephalomyelitis (EAE).

108 ey mediator of tmTNF-dependent protection in experimental autoimmune encephalomyelitis (EAE).

109 ultiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).

110 suppress progression of relapsing-remitting experimental autoimmune encephalomyelitis (EAE).

111 rine Th1 cell- and Th17 cell-driven model of experimental autoimmune encephalomyelitis (EAE).

112 central nervous system (CNS) inflammation in experimental autoimmune encephalomyelitis (EAE).

113 on of Nrf2 in DMF treatment of the MS model, experimental autoimmune encephalomyelitis (EAE).

114 godendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis (EAE).

115 n the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis (EAE).

116 and their disease-modulating activity on the Experimental Autoimmune Encephalomyelitis (EAE).

117 ) attenuates chronic and relapsing-remitting experimental autoimmune encephalomyelitis (EAE).

118 clerosis (MS) and of its rodent counterpart, experimental autoimmune encephalomyelitis (EAE).

119 or the proinflammatory cytokine IFN-gamma in experimental autoimmune encephalomyelitis (EAE).

120 in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE).

121 s in more severe pathogenesis of colitis and experimental autoimmune encephalomyelitis (EAE).

122 of pT(reg) cells, and decreased severity of experimental autoimmune encephalomyelitis (EAE).

123 e in a neuroinflammatory autoimmunity model, experimental autoimmune encephalomyelitis (EAE).

124 n the SJL mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE).

125 immune responses and are more susceptible to experimental autoimmune encephalomyelitis (EAE).

126 n the multiple sclerosis (MS) mouse model of experimental autoimmune encephalomyelitis (EAE).

127 affected by chronic inflammation modeled by experimental autoimmune encephalomyelitis (EAE).

128 ll-mediated demyelinating autoimmune disease experimental autoimmune encephalomyelitis (EAE).

129 pathogenesis of autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE).

130 n oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE).

131 electively enriched in the CNS tissue during experimental autoimmune encephalomyelitis (EAE).

132 ltiple sclerosis (MS) and of its mouse model experimental autoimmune encephalomyelitis (EAE).

133 d with a murine model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE).

134 M-SOB on susceptibility of C57BL/6J mice to experimental autoimmune encephalomyelitis (EAE).

135 ding multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE).

136 f S1P1 in Th17 cells conferred resistance to experimental autoimmune encephalomyelitis (EAE).

137 and can also suppress the manifestations of experimental autoimmune encephalomyelitis (EAE).

138 nflammation, such as the spinal cord, during experimental autoimmune encephalomyelitis (EAE).

139 astrocytes in the most widely used MS model, experimental autoimmune encephalomyelitis (EAE).

140 o create effective ASIT for the treatment of experimental autoimmune encephalomyelitis (EAE).

141 l cells in both human MS and the mouse model experimental autoimmune encephalomyelitis (EAE).

142 ultiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).

143 cells during autoimmune responses, including experimental autoimmune encephalomyelitis (EAE).

144 G peptide resulted in attenuated severity of experimental autoimmune encephalomyelitis (EAE).

145 in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE).

146 nflammation and autoimmune diseases, such as experimental autoimmune encephalomyelitis (EAE); however

147 ultiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE); however

148 cause exacerbated ascending paralysis during experimental autoimmune encephalomyelitis (EAE); instead

149 utoimmune cells that attack myelin sheath in experimental autoimmune encephalomyelitis (EAE, an anima

150 sue during neuroinflammation associated with experimental autoimmune encephalomyelitis (EAE; a mouse

151 cidation of factors influencing the onset of experimental autoimmune encephalomyelitis (eg, susceptib

152 ne Th1 and Th17 cells independently transfer experimental autoimmune encephalomyelitis (widely used a

153 PHTPP-mediated experimental autoimmune encephalomyelitis amelioration w

154 CD99 blockade in vivo ameliorated experimental autoimmune encephalomyelitis and decreased

155 X2 were partially protected from MOG-induced experimental autoimmune encephalomyelitis and displayed

156 thermore, CD43(-/-) mice were protected from experimental autoimmune encephalomyelitis and had impair

157 or CaV3.1 were resistant to the induction of experimental autoimmune encephalomyelitis and had reduce

158 Mas deficiency exacerbated the course of experimental autoimmune encephalomyelitis and increased

159 al outcome in a relapsing/remitting model of experimental autoimmune encephalomyelitis and is neuropr

160 the blood-brain barrier that occurs in both experimental autoimmune encephalomyelitis and multiple s

161 of mir-181a-1/b-1 dampened the induction of experimental autoimmune encephalomyelitis and reduced ba

162 ree mice resulted in more severe symptoms of experimental autoimmune encephalomyelitis and reduced pr

163 salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis and salt-sensi

164 iRNA established protective immunity against experimental autoimmune encephalomyelitis and suppressed

165 anolipogel delivery system, markedly reduced experimental autoimmune encephalomyelitis and was 10-fol

166 mage and preserve neurologic function in the experimental autoimmune encephalomyelitis animal model o

167 ntravenous injection of IL4I1 into mice with experimental autoimmune encephalomyelitis at disease ons

168 ublic repertoire representation in mice with experimental autoimmune encephalomyelitis at high resolu

169 acked functional synergy with MOG to promote experimental autoimmune encephalomyelitis because NFM-de

170 se results demonstrate that MEDI551 disrupts experimental autoimmune encephalomyelitis by inhibiting

171 ly improved protection from MOG35-55-induced experimental autoimmune encephalomyelitis compared with

172 In an experimental autoimmune encephalomyelitis disease model

173 in-specific Kv1.3-KO Th cells can ameliorate experimental autoimmune encephalomyelitis following tran

174 GOT1 with (aminooxy)acetic acid ameliorated experimental autoimmune encephalomyelitis in a therapeut

175 to bisphenol-A increased the development of experimental autoimmune encephalomyelitis in adulthood i

176 ated T cells and shows inhibitory effects on experimental autoimmune encephalomyelitis in both preven

177 Treatment with ACs reduces the severity of experimental autoimmune encephalomyelitis in hosts with

178 Moreover, experimental autoimmune encephalomyelitis in mice lackin

179 duction in vitro and in vivo and ameliorates experimental autoimmune encephalomyelitis in mice.

180 , and in addition, inhibition of GSK3 limits experimental autoimmune encephalomyelitis in mice.

181 mod (FTY720) ameliorated chronic progressive experimental autoimmune encephalomyelitis in nonobese di

182 st the subsequent development of MOG-induced experimental autoimmune encephalomyelitis in vivo.

183 mer-positive T cells and promoted consistent experimental autoimmune encephalomyelitis induction, unl

184 ) T cells and monocytes expressed ANKRD55 in experimental autoimmune encephalomyelitis mice, with the

185 adjuvant arthritis model (AA) and the mouse experimental autoimmune encephalomyelitis model (EAE).

186 In an in vivo experimental autoimmune encephalomyelitis model in which

187 es clinical disease when administered in the experimental autoimmune encephalomyelitis model of MS.

188 We reported in a nonhuman primate experimental autoimmune encephalomyelitis model that an

189 ious in reducing disease severity in a mouse experimental autoimmune encephalomyelitis model, demonst

190 red after priming using an adoptive transfer experimental autoimmune encephalomyelitis model.

191 /PD) mice were protected in a Th17-dependent experimental autoimmune encephalomyelitis model.

192 f the two drugs at the peak of disease in an experimental autoimmune encephalomyelitis mouse model of

193 cytes leads to phenotypes reminiscent of the experimental autoimmune encephalomyelitis mouse model wi

194 led to exacerbated neuroinflammation in the experimental autoimmune encephalomyelitis mouse model.

195 A new generation of spontaneous experimental autoimmune encephalomyelitis mouse models h

196 4 were impaired in their ability to suppress experimental autoimmune encephalomyelitis or islet allog

197 spinal cords and kidneys of mice developing experimental autoimmune encephalomyelitis or lupus, resp

198 vivo, RGC-32(-/-) mice display an attenuated experimental autoimmune encephalomyelitis phenotype acco

199 ion and the consequences of treatment in the experimental autoimmune encephalomyelitis rat model.

200 We show in this article that TSSP increases experimental autoimmune encephalomyelitis severity by li

201 The effect on experimental autoimmune encephalomyelitis severity was M

202 Gpr174(-/Y) mice were less susceptible to experimental autoimmune encephalomyelitis than wild-type

203 Eos(-/-) mice developed more severe experimental autoimmune encephalomyelitis than WT mice,

204 icantly reduced active and adoptive-transfer experimental autoimmune encephalomyelitis that is charac

205 It has been demonstrated that during experimental autoimmune encephalomyelitis there are myel

206 atory Th17 cells because they induced severe experimental autoimmune encephalomyelitis upon adoptive

207 Clinical and histological experimental autoimmune encephalomyelitis was observed i

208 lyzed in a murine model of CNS autoimmunity (experimental autoimmune encephalomyelitis).

209 an experimental model of multiple sclerosis [experimental autoimmune encephalomyelitis, (EAE)] and a

210 cantly reduced throughout the progression of experimental autoimmune encephalomyelitis, a model for m

211 ttenuated disease in CD4(+) T cell-dependent experimental autoimmune encephalomyelitis, a mouse model

212 g MIF or D-DT developed less-severe signs of experimental autoimmune encephalomyelitis, a murine mode

213 tion in delayed-type hypersensitivity and in experimental autoimmune encephalomyelitis, an animal mod

214 ng into the spinal cord of mice subjected to experimental autoimmune encephalomyelitis, an animal mod

215 Importantly, EP had in vivo impact on experimental autoimmune encephalomyelitis, an animal mod

216 Kv1.3-knockout (KO) mice are protected from experimental autoimmune encephalomyelitis, an animal mod

217 ecific hypersensitivity reactions, relapsing experimental autoimmune encephalomyelitis, and antibody

218 ultiple sclerosis (MS), and its animal model experimental autoimmune encephalomyelitis, are neuroinfl

219 leviate and even prevent signs of disease in experimental autoimmune encephalomyelitis, as well as ma

220 myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, B7-H1-Ig exhi

221 lation, Apom(-/-) mice developed more severe experimental autoimmune encephalomyelitis, characterized

222 Remarkably, in experimental autoimmune encephalomyelitis, cholesterol s

223 lated immunity and protected animals against experimental autoimmune encephalomyelitis, decreasing Th

224 e of MEDI551, given before or during ongoing experimental autoimmune encephalomyelitis, disrupts deve

225 In experimental autoimmune encephalomyelitis, forced expres

226 In a mouse model of MS, experimental autoimmune encephalomyelitis, guanabenz all

227 When subjected to experimental autoimmune encephalomyelitis, IL-17R-signal

228 We report that, in an MS murine model of experimental autoimmune encephalomyelitis, miR-155 contr

229 rmatitis, and were resistant to induction of experimental autoimmune encephalomyelitis, presumably by

230 ysolecithin-induced demyelination as well as experimental autoimmune encephalomyelitis, principal ani

231 In experimental autoimmune encephalomyelitis, the animal mo

232 Using a murine model of multiple sclerosis, experimental autoimmune encephalomyelitis, we demonstrat

233 In stark contrast, using experimental autoimmune encephalomyelitis, we show that

234 nt autoimmune diseases such as arthritis and experimental autoimmune encephalomyelitis, where c-Rel p

235 it lesions in rhesus monkey brain induced by experimental autoimmune encephalomyelitis, which is the

236 s of PTEN-targeting APCs were protected from experimental autoimmune encephalomyelitis, which was acc

237 ed TH1 and TH17 immune responses are seen in experimental autoimmune encephalomyelitis.

238 ntiated antitumor responses, and exacerbated experimental autoimmune encephalomyelitis.

239 n was increased in the murine mouse model of experimental autoimmune encephalomyelitis.

240 cell lineage, but not immunopathology during experimental autoimmune encephalomyelitis.

241 lls, present in the circulation of mice with experimental autoimmune encephalomyelitis.

242 gen receptor (ER) beta ligands could inhibit experimental autoimmune encephalomyelitis.

243 vo, these mice exhibited reduced severity of experimental autoimmune encephalomyelitis.

244 on of a T cell-dependent autoimmune disease, experimental autoimmune encephalomyelitis.

245 7 cells, and consequently protects mice from experimental autoimmune encephalomyelitis.

246 ecifically in Th17 cells protected mice from experimental autoimmune encephalomyelitis.

247 of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis.

248 cribed to develop more aggressive courses of experimental autoimmune encephalomyelitis.

249 ulatory T cells) and enhance the severity of experimental autoimmune encephalomyelitis.

250 universally required for the development of experimental autoimmune encephalomyelitis.

251 as wild-type littermates to T cell-dependent experimental autoimmune encephalomyelitis.

252 oxp3(+) Tregs in WT mice and amelioration of experimental autoimmune encephalomyelitis.

253 z ameliorates relapse in relapsing-remitting experimental autoimmune encephalomyelitis.

254 d macrophages, and reduces susceptibility to experimental autoimmune encephalomyelitis.

255 s Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis.

256 -lymphoid tissues and impaired resolution of experimental autoimmune encephalomyelitis.

257 ucing the clinical symptoms and pathology of experimental autoimmune encephalomyelitis.

258 Similar changes are seen in mice with experimental autoimmune encephalomyelitis.

259 ing multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis.

260 sease in T cell transfer-induced colitis and experimental autoimmune encephalomyelitis.

261 in a skin hypersensitivity model and blocked experimental autoimmune encephalomyelitis.

262 o differentiation and in vivo development of experimental autoimmune encephalomyelitis.

263 inflamed central nervous system of mice with experimental autoimmune encephalomyelitis.

264 n of, and an immunotherapeutic reduction in, experimental autoimmune encephalomyelitis.

265 nglion cell damage in multiple sclerosis and experimental autoimmune encephalomyelitis.

266 oils, such as collagen-induced arthritis or experimental autoimmune encephalomyelitis.

267 rd of mice subjected to chronic or relapsing experimental autoimmune encephalomyelitis.

268 d chronic neurodegenerative phases of murine experimental autoimmune encephalomyelitis.

269 ent mice exhibited reduced susceptibility to experimental autoimmune encephalomyelitis.

270 rosis (MS) and a mouse model of the disease (experimental autoimmune encephalomyelitis; EAE), but the

271 otective effects in autoimmune diseases like experimental autoimmune encephalomyelitis; however, its

272 mice were protected from the development of experimental autoimmune encephalopathy, a model of the a

273 e peptides did not lead to clinical signs of experimental autoimmune glomerulonephritis or necrotizin

274 Mouse experimental autoimmune glomerulonephritis, a model of h

275 ore, studied the effect of SYK inhibition in experimental autoimmune GN, a rodent model of antiglomer

276 or SYK, completely prevents the induction of experimental autoimmune GN.

277 o have immunoregulatory functions in several experimental autoimmune models.

278 Myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG) are cau

279 effectively reversed disease progression in experimental autoimmune myasthenia gravis (EAMG), a T ce

280 In this study, we used the experimental autoimmune myocarditis (EAM) model to deter

281 Experimental autoimmune myocarditis (EAM) was initiated

282 ng the well-established model of TnI-induced experimental autoimmune myocarditis (EAM), we demonstrat

283 yet been studied in P0106-125-induced murine experimental autoimmune neuritis (EAN).

284 t been dissected in P0106-125-induced murine experimental autoimmune neuritis.

285 in the TLR signaling pathway, was studied in experimental autoimmune neuritis.

286 g.2098 is the dominant peptide when inducing experimental autoimmune thyroiditis (EAT) in NOD mice ex

287 d protect against the ocular inflammation in experimental autoimmune uveitis (EAU) mice through regul

288 merges in the spleen of mice recovering from experimental autoimmune uveitis (EAU), a murine model fo

289 Experimental autoimmune uveitis (EAU), in which CD4(+) T

290 nate, on uveitis using an inducible model of experimental autoimmune uveitis (EAU).

291 Moreover, the amelioration of experimental autoimmune uveitis in Il1r-deficient mice w

292 F8 deletion in T cells has no effect on EAE, experimental autoimmune uveitis is exacerbated in CD4-IR

293 fect on Th17 and Th1 autoimmune responses in experimental autoimmune uveitis, a mouse model of human

294 s of IL-1R signaling confers protection from experimental autoimmune uveitis.

295 at mesenchymal stem cells (MSCs) ameliorated experimental autoimmune uveoretinitis (EAU) in rats.

296 Experimental autoimmune uveoretinitis is a model for non

297 sis of the ocular infiltrate in WT mice with experimental autoimmune uveoretinitis showed a mixed pop

298 Experimental autoimmune uveoretinitis was dramatically r

299 tion of pathogenic type 17 helper T cells in experimental autoimmune uveoretinitis was reduced with G

300 of G-CSF in a murine model of human uveitis-experimental autoimmune uveoretinitis.